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Plasma β-Endorphin Levels in Primary Aldosteronism*

1985; Oxford University Press; Volume: 60; Issue: 2 Linguagem: Inglês

10.1210/jcem-60-2-315

1945-7197

George T. Griffing, Tracy K. McIntosh, Brian A. Berelowitz, Margo Hudson, Robert T. Salzman, Jo Ann E. Manson, James C. Melby,

Renin-Angiotensin System Studies

Excessive production of an as yet unidentified aldosterone-stimulating factor may cause idiopathic hyperaldosteronism (IHA). This putative factor may be related to proopiomelanocortin- derived peptides, some of which have aldosterone- stimulating properties. The present study evaluated plasma β-endorphin, ACTH, cortisol, and aldosterone levels in patients with IHA (n = 10), aldosterone-producing adenomas (n = 4), essential hypertension (n = 11), and normal subjects (n = 10). Plasma and urinary hormone measurementswere obtained at timed intervals during an isocaloric, fixed electrolyte intake (Na+, 128 meq/day; K+, 80 meq/day) in a metabolic unit. Plasma for β3-endorphin assay was preincubated with sepharose-bound anti-jS-lipotropin to remove j8-lipotropin that cross-reacted with theβ-endorpnin RIA. Mean ±SE plasma β-endorphin levels at 0800 h were elevated in IHA patients (47 ± 13 fmol/ml) compared to those in aldosterone-producing adenoma (25 ± 9), essential hypertension (16 ± 1), and normal control (20 ± 2; P < 0.05) subjects. Plasma ACTH, plasma cortisol, and urinary cortisol levels were not different in these four groups. These data support the hypothesis that excess production of either β- endorphin or related proopiomelanocortin-derived peptides may function as aldosterone secretogogue(s) in IHA.